Objectives To study the incidence and cerebral regional distribution of beta-amyloid plaques and angiopathy in the brains of autopsied rhesus monkeys from different age groups including late adult, perimenopausal, postmenopausal, and senescent ages. Beta-amyloid and amyloid precursor proteins in the plaques were detected by immunocytochemical staining. ABSTRACT:For a series of pathological studies of aged-related brain lesions, 81 brains of rhesus monkeys in different age groups were collected from autopsy cases performed in our Center during the past 14 years. Based on our previous studies on biosenescence and aged-related pathology of the macaques, the aged groups were divided as follows late adulthood (16 to 19 years), peri-menopausal (20 to 25 years), postmenopausal (26 to 31 years), and senescence (over 31 years). Using formalin-fixed brains, paraffin and frozen sections of the frontal, parietal, temporal, and occipital gyri, the amygdala, and the hippocampus were stained with the silver impregnation method and immunocytochemistry performed for beta-amyloid and amyloid precursor proteins. No amyloid plaques were found in the brains of 16- to 19-year-old macaques (8 cases). In aged groups, the average rates of the plaque or angiopathic lesions were 20. 8% in the 20- to 25-year group (24 cases), 60.9% in the 26- to 31-year group (41 cases), and 100%in the 33- to 39-year group (8 cases). Among 38 cases manifesting the amyloid plaque lesions, 10 were accompanied by amyloid angiopathy in the cerebral and meningeal blood vessels. The amyloid tissue in both the plaque and perivascular wall showed positive staining with beta-amyloid and amyloid precursor protein, and, ultrastructurally, the amyloid fibrilles were found in extraneuronal spaces of plaques and interstitial spaces of vascular smooth muscle cells. No neurofibrillary tangles were detected in these brain lesions. Twelve cases in the aged monkeys had an involvement of visceral amyloidosis in the liver, adrenal, or the pancreatic islets, and 7 of 12 had cerebral amyloidosis. The amyloid in the visceral organs showed no cross reactivity with beta-amyloid and precursor proteins. It appears that there is no pathogenetic correlation between cerebral and visceral amyloidosis. As in the aged human population, the aged macaque also spontaneously develops Alzheimer-type brain lesions. Keywords amyloid plaque Alzheimer lesion brain aged macaques